Dissections occur when the wall of a lumen tears, creating a secondary or false lumen. Blood can flow into this false lumen, generally causing the vessel to balloon outwardly as a result of the weaker lumen wall. If the dissection is left untreated, there is the risk of rupture of the lumen, with severe consequences to the patient. Dissections can be treated by open surgery, involving closing the tear by suturing and/or strengthening of the lumen wall, again often by suturing. Open surgery procedures should, however, preferably avoided, particularly to the thoracic region, in light of the trauma caused to the patient. For this purpose, some endoluminal treatments have been developed in which the dissection is treated by means of a stent or stent graft placed against the damaged portion of the vessel wall. The stent or stent graft acts to press together the two parts of the lumen wall so as to close off the false lumen. It has been found that if the false lumen can be closed, the lumen wall often repairs itself. A stent graft can usefully be placed at the point of the tear, so as to close off the blood supply to the false lumen. This removes the blood pressure in the false lumen and thus allows the two parts of the lumen wall to come into contact one another and thus to heal in time.
The use of stents and stent grafts to treat dissections has been restricted to lumen locations and zones which are free of complications, such as branch vessels, complex lumen geometries and so on, particularly in light of the difficulties in placing the stent and stent grafts accurately in the lumen. As a result of the particular complexities of Type-A dissections, that is dissections in the ascending aorta, stents or stent grafts have not been used. At this location, there is only a short length of aorta which is free of side branches critical to the health of the patient. The geometry of the lumen that is beyond the aortic arch also causes positioning difficulties.
More particularly, a Type-A thoracic aorta dissection (TAD-A) is a condition in which the intimal layer of the ascending thoracic aorta develops a tear, allowing blood to flow into the layers of the aortic wall, causing the development of medial or subintimal hematoma. TAD-A is associated with a very high mortality rate of around 1 to 2% per hour for the first 48 hours. Currently, the only option for treatment of TAD-As is open surgical repair which includes opening the chest cavity, clamping the aorta and sewing a vascular prosthesis in place. Operative mortality rate for TAD-A is significant at approximately 10%.
The ability to treat a TAD-A quickly is imperative but current procedures are lengthy, invasive and associated with high morbidity and mortality. The ability to treat TAD-As through endovascular procedures would represent a significant step forward and reduction in mortality rates. However, the ascending aortic arch is complex by reason of the coronary arteries and brachiocephalic artery and that any obstruction of these can lead to patient demise. As a result of this, the treatment of Type-A dissections and other vascular defects in the ascending aorta still remains restricted to open surgical procedures.